Two strains of mice, LT/Sv and 129 Sv, produce spontaneous ovarian and testicular teratomas, respectively. These teratomas, which arise from primordial germ cells in the gonads, probably represent a form of parthenogenetic development since ova from female LT/Sv mice also develop parthenogenetically after superovulation. This later circumstance allows us to ask whether genetic events such as X chromosome inactivation, which occurs early in normal development, also occurs during pathenogenesis. Since a biochemical method to detect the time of X chromosome inactivation has not yet been demonstrated, we have concentrated on devloping a new approach to this problem. Our approach is based upon the observation that the flycolytic enzymes that cone vert dihysroxyacetone phosphate to phosphoenol pyruvate are present in cells in equimolar concentrations and also are coded for by genes located both on autosomes and on the X chromosome. Accordingly, the ratios of these enzymes to one another will vary whether one or two X chromosomes are active. We hope, therefore, to detect the time of X chromosome inactivation in normal embryonic and teratocarcinogenetic development. In addition, we intend to sue the method to assess whether one or two X chromosomes are active in the germ cells of the genital ridge before meiosis occurs. If our initial premise is correct and provides us with information as to the time at which major genetic changes are occurring in the early stages of teratoma development, we will subsequently characterize cyclic AMP regulation in teratomas during these critical stages. These experiments are being pursued both in vivo and in vitro.